Search results for "Immunoglobulin heavy chain"

showing 10 items of 15 documents

Ibrutinib, obinutuzumab, and venetoclax in relapsed and untreated patients with mantle cell lymphoma: a phase 1/2 trial.

2020

Abstract Ibrutinib, obinutuzumab, and venetoclax demonstrate synergy in preclinical models of mantle cell lymphoma (MCL). OAsIs (NCT02558816), a single-arm multicenter prospective phase 1/2 trial, aimed to determine the maximum tolerated dose of venetoclax in combination with fixed doses of ibrutinib and obinutuzumab, in relapsed MCL patients. At the venetoclax MTD, extension cohorts were opened for relapsed and untreated patients. Safety and efficacy were secondary objectives. Minimal residual disease (MRD) was assessed by allele-specific oligonucleotide quantitative polymerase chain reaction. Between 14 October 2015 and 29 May 2018, 48 patients were enrolled. No dose-limiting toxicity was…

0301 basic medicineMaleNeoplasm Residualmedicine.medical_treatmentImmunoglobulin Variable RegionHematopoietic stem cell transplantationKaplan-Meier EstimateLymphoma Mantle-CellBiochemistryGastroenterologychemistry.chemical_compound0302 clinical medicinePiperidinesObinutuzumabAntineoplastic Combined Chemotherapy ProtocolsProspective StudiesProspective cohort studyAged 80 and overSulfonamidesHematopoietic Stem Cell TransplantationHematologyMiddle AgedCombined Modality TherapyProgression-Free Survival3. Good healthTreatment Outcome030220 oncology & carcinogenesisIbrutinibFemaleImmunoglobulin Heavy Chainsmedicine.medical_specialtyMaximum Tolerated DoseImmunologyAntibodies Monoclonal Humanized03 medical and health sciencesInternal medicinemedicineHumansProgression-free survivalAgedVenetoclaxbusiness.industryAdenineCell Biologymedicine.diseaseBridged Bicyclo Compounds HeterocyclicGenes p53Minimal residual diseaseHematologic Diseases030104 developmental biologychemistryMutationMantle cell lymphomabusinessFollow-Up StudiesBlood
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CD38-Specific Biparatopic Heavy Chain Antibodies Display Potent Complement-Dependent Cytotoxicity Against Multiple Myeloma Cells

2018

CD38 is overexpressed by multiple myeloma cells and has emerged as a target for therapeutic antibodies. Nanobodies are soluble single domain antibody fragments derived from the VHH variable domain of heavy chain antibodies naturally occurring in camelids. We previously identified distinct llama nanobodies that recognize three non-overlapping epitopes of the extracellular domain of CD38. Here, we fused these VHH domains to the hinge, CH2, and CH3 domains of human IgG1, yielding highly soluble chimeric llama/human heavy chain antibodies (hcAbs). We analyzed the capacity of these hcAbs to mediate complement-dependent cytotoxicity (CDC) to CD38-expressing human multiple myeloma and Burkitt lymp…

0301 basic medicinelcsh:Immunologic diseases. AllergyRecombinant Fusion ProteinsImmunologyAntineoplastic AgentsEpitope03 medical and health sciencesbiparatopic antibodiesAntigens Neoplasmhemic and lymphatic diseasesCell Line TumorAntibodies BispecificImmunology and AllergyAnimalsHumansCytotoxicitycomplement-dependent cytotoxicityOriginal ResearchHeavy-chain antibodybiologyheavy chain antibodyantibody engineeringChemistryAntibody-Dependent Cell CytotoxicityDaratumumabAntibodies MonoclonalComplement System ProteinsSingle-Domain AntibodiesADP-ribosyl Cyclase 1Complement-dependent cytotoxicityCell biologymultiple myelomananobody030104 developmental biologySingle-domain antibodyCell culturebiology.proteinEpitopes B-LymphocyteImmunotherapyAntibodylcsh:RC581-607Immunoglobulin Heavy ChainsCamelids New WorldCD38Frontiers in Immunology
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Incidence of lineage promiscuity in acute myeloblastic leukemia: Diagnostic implications of immunoglobulin and T-cell receptor gene rearrangement ana…

1988

Abstract Sixty-nine blood or bone marrow samples from both children and adults with acute myeloblastic leukemia (AML) were investigated to elucidate the frequency of immunoglobulin (IG) and T-cell receptor (TCR)-gene rearrangements. Non-germline configuration for the IG heavy chain (h) gene was detected in the specimens of nine patients of various subtypes according to the French-American-British classification (FAB), including FAB M1, M2, M4 and M5. Rearrangement of the IG kappa chain (k) gene was present in one of these cases which simultaneously revealed a rearranged TCR-beta (b) chain gene. In another two AML samples we found TCR-b gene rearrangements, in one case in combination with an…

AdultImmunoglobulin geneCancer ResearchAcute myeloblastic leukemiaCD19medicineHumansGene Rearrangement beta-Chain T-Cell Antigen ReceptorChildGenes ImmunoglobulinbiologyAntibodies MonoclonalCell DifferentiationHematologyGene rearrangementmedicine.diseaseMolecular biologyLeukemia Myeloid AcuteLeukemiaPhenotypeOncologyTerminal deoxynucleotidyl transferaseT-Cell Receptor Genebiology.proteinAntibodyImmunoglobulin Heavy ChainsLeukemia Research
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Analysis of chronic lymphotic leukemia transcriptomic profile: differences between molecular subgroups

2009

B cell chronic lymphocytic leukemia (CLL) is a lymphoproliferative disorder with a variable clinical course. Patients with unmutated IgV(H) gene show a shorter progression-free and overall survival than patients with immunoglobulin heavy chain variable regions (IgV(H)) gene mutated. In addition, BCL6 mutations identify a subgroup of patients with high risk of progression. Gene expression was analysed in 36 early-stage patients using high-density microarrays. Around 150 genes differentially expressed were found according to IgV(H) mutations, whereas no difference was found according to BCL6 mutations. Functional profiling methods allowed us to distinguish KEGG and gene ontology terms showing…

AdultMaleCancer ResearchBCL6BiologyIgVHgenomichemic and lymphatic diseasesmedicineHumansKEGGGenemicroarraysAgedAged 80 and overRegulation of gene expressionGeneticsB-LymphocytesGene Expression ProfilingZAP70HematologyMiddle Agedmedicine.diseaseBCL6Leukemia Lymphocytic Chronic B-CellDNA-Binding ProteinsGene Expression Regulation NeoplasticGene expression profilingLeukemiaOncologyTranscriptomicHealthMutationProto-Oncogene Proteins c-bcl-6Cancer researchImmunoglobulin heavy chainFemaleImmunoglobulin Heavy ChainsCLL
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BCL6: somatic mutations and expression in early-stage chronic lymphocytic leukemia

2009

BCL6 somatic mutations affect normal and tumoral post germinal center B-lymphocytes. Our objective was to analyse expression, mutations and polymorphisms in the BCL6 gene and to correlate those variables with the clinical outcome in early-stage chronic lymphocytic leukemia (CLL). CLL samples were used for characterisation of the mutational status of BCL6/ immunoglobulin variable heavy chain (IGHV) genes, and expression of BCL6 was determined by real time PCR and immunoblot. Out of 68 cases, 29% show somatic mutations on BCL6 which occur exclusively in IGHV mutated cases. They are single nucleotide substitutions located mainly in two short mutational hot spots. CLL cells express different le…

AdultMaleCancer ResearchSomatic cellChronic lymphocytic leukemiaBiologyPredictive Value of Testsimmune system diseaseshemic and lymphatic diseasesmedicineHumansPoint MutationGeneAgedAged 80 and overPolymorphism GeneticGenes ImmunoglobulinGerminal centerHematologyMiddle AgedPrognosismedicine.diseaseBCL6Leukemia Lymphocytic Chronic B-CellDNA-Binding ProteinsTreatment OutcomeReal-time polymerase chain reactionOncologyMutationImmunologyProto-Oncogene Proteins c-bcl-6biology.proteinFemaleAntibodyImmunoglobulin Heavy ChainsIGHV@Leukemia & Lymphoma
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Molecular Basis for the Interaction of the Hepatitis B Virus Core Antigen with the Surface Immunoglobulin Receptor on Naive B Cells

2001

ABSTRACTThe nucleocapsid of the hepatitis B virus (HBV) is composed of 180 to 240 copies of the HBV core (HBc) protein. HBc antigen (HBcAg) capsids are extremely immunogenic and can activate naive B cells by cross-linking their surface receptors. The molecular basis for the interaction between HBcAg and naive B cells is not known. The functionality of this activation was evidenced in that low concentrations of HBcAg, but not the nonparticulate homologue HBV envelope antigen (HBeAg), could prime naive B cells to produce anti-HBc in vitro with splenocytes from HBcAg- and HBeAg-specific T-cell receptor transgenic mice. The frequency of these HBcAg-binding B cells was estimated by both hybridom…

CD4-Positive T-LymphocytesImmunologyNaive B cellAntigen presentationMolecular Sequence DataImmunoglobulin Variable RegionMice Transgenicmedicine.disease_causeAntibodies ViralMicrobiologyMiceAntigenVirologymedicineAnimalsHumansAmino Acid SequenceReceptors ImmunologicHepatitis B virusAntigen PresentationB-LymphocytesMice Inbred BALB Cbiologyvirus diseasesAntibodies MonoclonalVirologyMolecular biologyHepatitis B Core Antigensdigestive system diseasesPeptide FragmentsVirus-Cell InteractionsHBcAgHBeAgImmunoglobulin MImmunoglobulin MInsect Sciencebiology.proteinMice Inbred CBAImmunoglobulin Light ChainsBinding Sites AntibodyAntibodyImmunoglobulin Heavy ChainsSequence Alignment
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Multiple levels of MHC class I down-regulation by ras oncogenes.

1996

A number of tumours and oncogene transformed cells displayed reduced MHC class I surface expression which seemed to enable their escape from immune surveillance. To test whether oncogenic activation is directly involved in suppressing MHC class I expression, a model of inducible oncogene expression was chosen. Mouse fibroblasts transfected with different oncogenes expressed under the control of the dexamethasone-inducible MMTV promoter were analysed in the presence and absence of hormone for the mRNA and protein expression of MHC class I molecules as well as the respective oncogenes. Immunofluorescence analyses demonstrated an inverse association of MHC class I and oncogene expression after…

CD74Transcription GeneticImmunologyCD1Down-RegulationGene ExpressionC-C chemokine receptor type 7TransfectionDexamethasoneMiceAntigenMHC class IAnimalsRNA Processing Post-TranscriptionalPromoter Regions GeneticMessenger RNAbiologyOncogeneHistocompatibility Antigens Class IGeneral Medicine3T3 CellsMHC restrictionMolecular biologyGenes rasMammary Tumor Virus MouseAntigens Surfacebiology.proteinImmunoglobulin Heavy Chainsbeta 2-MicroglobulinScandinavian journal of immunology
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Immunoadhesins of interleukin-6 and the IL-6/soluble IL-6R fusion protein hyper-IL-6.

1999

Signal transduction in response to interleukin-6 (IL-6) results from homodimerization of gp130. This dimerization occurs after binding of IL-6 to its surface receptor (IL-6R) and can also be triggered by the complex of soluble IL-6R and IL-6. We fused IL-6 to the constant region of a human IgG1 heavy chain (Fc). IL-6Fc was expressed in COS-7 cells and purified via Protein A Sepharose. Using three different assays we found that the biological activity of this dimeric IL-6 protein is comparable with monomeric IL-6. Recently, we described the designer cytokine Hyper-IL-6 (H-IL-6) in which soluble IL-6R and IL-6 are connected via a flexible peptide linker. This molecule turned out to be 100-100…

Carcinoma HepatocellularRecombinant Fusion ProteinsImmunologyBiologyProtein EngineeringMiceTumor Cells CulturedImmunology and AllergyAnimalsHumansReceptorCOS cellsInterleukin-6HydrolysisThrombinBiological activityProtein engineeringGlycoprotein 130Fusion proteinReceptors Interleukin-6In vitroImmunoglobulin Fc FragmentsBiochemistryImmunoglobulin GCOS CellsSignal transductionImmunoglobulin Heavy ChainsDimerizationJournal of immunological methods
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Impact of a Three Amino Acid Deletion in the CH2 Domain of Murine IgG1 on Fc-Associated Effector Functions

2008

Abstract Four murine IgG subclasses display markedly different Fc-associated effector functions because of their differential binding to three activating IgG Fc receptors (FcγRI, FcγRIII, and FcγRIV) and C1q. Previous analysis of IgG subclass switch variants of 34-3C anti-RBC monoclonal autoantibodies revealed that the IgG1 subclass, which binds only to FcγRIII and fails to activate complement, displayed the poorest pathogenic potential. This could be related to the presence of a three amino acid deletion at positions 233–235 in the CH2 domain uniquely found in this subclass. To address this question, IgG1 insertion and IgG2b deletion mutants at positions 233–235 of 34-3C anti-RBC Abs were …

Deletion mutantImmunologyAntibody AffinityDown-Regulationddc:616.07BiologySubclassProtein Structure Tertiary/geneticsMiceAnimalsImmunology and AllergyAmino AcidsEffector functionsSequence DeletionMice Knockoutchemistry.chemical_classificationMice Inbred BALB CMice Inbred NZBAnemia Hemolytic Autoimmune/genetics/immunologyReceptors IgGAutoantibodyAmino Acids/chemistry/genetics/metabolismIgg subclassesReceptors IgG/antagonists & inhibitors/genetics/metabolismPathogenicityProtein Structure TertiaryImmunoglobulin G/genetics/metabolismImmunoglobulin Switch RegionCell biologyAmino acidImmunoglobulin Heavy Chains/biosynthesis/genetics/metabolismAntibody Affinity/geneticsBiochemistrychemistryImmunoglobulin GMonoclonalMutagenesis Site-DirectedAnemia Hemolytic AutoimmuneDown-Regulation/genetics/immunologyImmunoglobulin Heavy ChainsThe Journal of Immunology
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Over 30% of patients with splenic marginal zone lymphoma express the same immunoglobulin heavy variable gene: ontogenetic implications.

2012

We performed an immunogenetic analysis of 345 IGHV-IGHD-IGHJ rearrangements from 337 cases with primary splenic small B-cell lymphomas of marginal-zone origin. Three immunoglobulin (IG) heavy variable (IGHV) genes accounted for 45.8% of the cases (IGHV1-2, 24.9%; IGHV4-34, 12.8%; IGHV3-23, 8.1%). Particularly for the IGHV1-2 gene, strong biases were evident regarding utilization of different alleles, with 79/86 rearrangements (92%) using allele *04. Among cases more stringently classified as splenic marginal-zone lymphoma (SMZL) thanks to the availability of splenic histopathological specimens, the frequency of IGHV1-2*04 peaked at 31%. The IGHV1-2*04 rearrangements carried significantly lo…

Immunoglobulin geneModels MolecularCancer ResearchGenes Immunoglobulin Heavy ChainGene Rearrangement B-Lymphocyte Heavy ChainImmunoglobulin Variable RegionSomatic hypermutationSplenic NeoplasmBiologyCohort StudiesantigenmedicineHumansSplenic marginal zone lymphomaAlleleGeneticsSplenic Neoplasmssplenic marginal-zone lymphomaHematologyGene rearrangementLymphoma B-Cell Marginal Zonemedicine.diseasePrognosisComplementarity Determining Regionssomatic hypermutationimmunoglobulin geneOncologyMutationIGHDsplenic marginal-zone lymphoma; immunoglobulin gene; somatic hypermutation; CDR3; antigenCDR3IGHV@Leukemia
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